Acupuncture is used to manage high blood pressure (BP) in clinical practice. However, the mechanisms underlying its hypotensive effects remain unclear. Our previous studies have shown that electroacupuncture (EA) at the ST36‐37 acupoints, overlying the deep peroneal nerve, attenuates pressor responses through adenosine A2A receptors (A2AR) in the rostral ventrolateral medulla (rVLM). A2AR activation in the rVLM is associated with the upregulation of nitric oxide synthase (NOS) that contributes to sympathoinhibition and BP reduction. However, it is uncertain whether rVLM A2AR contributes to EA’s action in lowering high BP in sustained hypertension (HTN) in the rVLM. We hypothesized that EA lowers BP in HTN through adenosine A2AR mechanisms associated with the upregulation of neuronal NOS (nNOS) in the rVLM. The nNOS derived NO has been shown to exert central effects on BP. To mimic essential HTN in the clinic, we performed EA in conscious Dahl salt‐sensitive hypertensive rat (DSHR). EA (0.1‐0.4 mA, 2 Hz) was applied at ST36‐37 for 30 min twice weekly for four weeks while sham‐EA was conducted with the same procedures as EA except for no electrical stimulation. Elevated BP was reduced by EA (n=10) but not sham‐EA (n=8) and untreated ones (n=6). The A2AR level in the rVLM after EA treatment was increased (n=5; P < 0.05) compared to the sham‐EA (n=5). EA’s inhibitory effect on elevated BP was reversed transiently by unilateral microinjection of SCH 58261 (1 mM in 50 nl; an A2AR antagonist; n=7; P < 0.05) but not the vehicle (n=5) into the rVLM in EA‐treated DSHRs under anesthesia. Activation of rVLM A2AR in DSHRs treated with sham‐EA using an A2AR agonist, CGS‐21680 (0.4 mM in 50 nl; n=6), decreased BP. Furthermore, we found a co‐localization of A2AR with nNOS in the rVLM of DSHRs. The expression of rVLM nNOS was enhanced in DSHRs treated with EA compared to those treated with sham‐EA (n=5 in each group; P < 0.05). These data suggest that adenosine‐ A2AR in the rVLM contributes to EA’s inhibitory effect on elevated BP in sustained HTN, which is likely relevant to the upregulation of nNOS.
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